English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Treatment of rabbit aortic endothelial cells or human umbilical vein cells for as little as 1 day with 25 micrograms/ml of beta-migrating very low density lipoprotein (beta-VLDL), but not low density lipoprotein (LDL), caused an increased binding of human peripheral blood monocytes to the endothelium. This increase was maximal by 24 hours but was not significant at 4 hours of pre-incubation with beta-VLDL. Neutrophil binding was not significantly stimulated by beta-VLDL treatment of endothelial cells, while endotoxin (LPS) treatment of endothelial cells stimulated both neutrophil and monocyte binding. Antibody to leukocyte function-associated-antigen-1 and to Mo2 inhibited binding to both beta-VLDL-stimulated and LPS-stimulated cells by 25%. The fact that both rabbit and human cells were stimulated by beta-VLDL to bind human monocytes suggests that some mechanisms regulating binding are conserved between species. These studies suggest that beta-VLDL acts like a chronic inflammatory mediator to cause a sustained increase in binding of monocytes to the endothelium.

Beta-very low density lipoprotein pretreatment of endothelial monolayers increases monocyte adhesion.